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GFI1 downregulation promotes inflammation-linked metastasis of colorectal cancer.
AMPK (show PRKAA1 Proteins) was sufficient to stimulate osteogenesis of MC3T3-E1 cells and inhibit adipogenesis of 3T3-L1 cells through the AMPK (show PRKAA1 Proteins)-Gfi1-OPN (show SPP1 Proteins) axis.
Gfi1 disruption antagonized the tumor-promoting effects of Ezh2 (show EZH2 Proteins) loss; conversely, Gfi1 overexpression collaborated with Myc (show MYC Proteins) to bypass effects of Trp53 (show TP53 Proteins) inactivation in driving medulloblastoma progression in primary cerebellar neuronal progenitors.
If Gfi1 levels fall below a threshold, Id1 (show ID1 Proteins) expression increases and renders E2A (show TCF3 Proteins) unable to function, which prevents hematopoietic progenitors from engaging along the B lymphoid lineage
These results clearly demonstrate that Gfi1 is a critical transcriptional regulator that controls the development of CD4pos and NK1.1pos Invariant natural killer T cells.
this study demonstrates the critical role of Gfi1 in the regulation of myeloid cells, and prevention of spontaneous lupus autoimmunity by negatively controlling TLR7 (show TLR7 Proteins) signaling
these findings demonstrate a novel regulatory role of Gfi1 in the regulation of the Th1 (show HAND1 Proteins)-type immune response.
GFI1 proteins recruit the chromatin-modifying protein LSD1 (show KDM1A Proteins), a member of the CoREST (show Rcor2 Proteins) repressive complex, to epigenetically silence the endothelial program in haemogenic endothelium and allow the emergence of blood cells
GFI1 inhibits NLRP3 (show NLRP3 Proteins) inflammasome activation and IL-1beta (show IL1B Proteins) secretion in macrophages
Gfi-1 is linked to the erythroid gene regulatory network by repressing Id2 expression.
Simvastatin attenuates the tumor-associated macrophage mediated gemcitabine resistance of PDAC by blocking the TGF-beta1/Gfi-1 axis.
combination of the sequence-specific and nonspecific DNA-binding modes of SATB1 (show SATB1 Proteins) should be advantageous in a search for target loci during transcriptional regulation
GFI1(36S) homozygous patients exhibited a sustained response to treatment with hypomethylating agents, whereas GFI1(36N) patients had a poor sustained response to this therapy. Because allele status of GFI1(36N) is readily determined using basic molecular techniques, we propose inclusion of GFI1(36N) status in future prospective studies for MDS (show PAFAH1B1 Proteins) patients to better predict prognosis and guide therapeutic decisions.
Maternal-smoking sensitive CpG sites in newborns were significantly associated with cg18146737 SNP located proximal to GFI1.
In this study, the influence of prenatal smoking exposure on the childrens' DNA methylation (show HELLS Proteins) state of a CpG island located upstream of the promoter of the growth factor independent 1 (GFI1) gene was analyzed. Significant hypomethylation was observed in this CpG island in SIDS (show IDS Proteins) cases with cigarette smoke exposure compared to non-exposed cases.
Gfi1 gene expression is regulated by cytokines in activated T cells.
miR-495 directly interacts with the Gfi1 3'UTR to regulate Gfi1 at a post-transcriptional level and the expression level of miR-495 is inversely correlated with the Gfi1 protein level in medulloblastoma specimens.
Gfi1 acts as a transcriptional repressor by recruiting histone-modifying enzymes to promoters and enhancers of target genes. Mutations of the C-terminal zinc finger domain causes congenital neutropenia. It may be involved in leukemia and lymphoma. Review.
During infection, the incoming HCMV rapidly downregulates the GFI1 mRNA and protein in both wild-type cells and in cells in which EZH2 (show EZH2 Proteins), NDY1/KDM2B (show KDM2B Proteins) or JARID2 (show JARID2 Proteins) were knocked down.
This gene encodes a nuclear zinc finger protein that functions as a transcriptional repressor. This protein plays a role in diverse developmental contexts, including hematopoiesis and oncogenesis. It functions as part of a complex along with other cofactors to control histone modifications that lead to silencing of the target gene promoters. Mutations in this gene cause autosomal dominant severe congenital neutropenia, and also dominant nonimmune chronic idiopathic neutropenia of adults, which are heterogeneous hematopoietic disorders that cause predispositions to leukemias and infections. Multiple alternatively spliced variants, encoding the same protein, have been identified for this gene.
growth factor independent protein 1
, zinc finger protein Gfi-1
, growth factor independence-1
, zinc finger protein 163
, growth factor independence 1
, Growth factor independent-1